This document discusses color vision and color blindness. It begins by describing the three types of cones in the eye that are sensitive to long, middle, and short wavelengths of light, corresponding to red, green, and blue colors. It explains that color vision is achieved through the trichromatic theory, with colors resulting from different combinations of the three primary colors stimulating the cones. The document also discusses color opponent processing and color blindness, outlining different types like dichromacy and anomalous trichromacy that affect color perception. Tests for color blindness like Ishihara plates are also mentioned.

1. BY-
DR.RAHUL PANDEY

2. Is the ability of the eye to discriminate between
colours excited by light of different wave lengths.

3. The sensation of colour is
subjective and it is a perceptual
phenomenon.
There are three different type of
cones.
 Red sensitive (725 – 647 nm)-
L(Long)
 Green sensitive (575 –
492nm)-M(Middle)
 Blue sensitive (492 – 450 nm)
- S(Short)

4. For any colour there is a
complementary color and if
properly mixed with it
produces a sensation of
white.
In Dim light all the colours
are seen as gray. This is
called “purkinje shift
phenomenon

5. THEORIES OF COLOUR VISION
 I. TRICHROMATIC THEORY:
Also called as young - helmholtz
theory
 It postulates the existence of
three kinds of cones
 Each cone containing a
different photopigment and
maximally sensitive to one of
three primary colours i.e. Red,
Green and Blue.
Thomas Young
Helmholtz

6.  A given colour consist of admixture of the three
primary colour in different proportion.eg.-
Computer moniters and Televisions.
 This theory has now been demonstrated by the
identification and chemical characterization of
each of the three pigments by recombinant DNA
technique.

7.  RED SENSITIVE
CONE PIGMENT
– (Erythrolabe
or long
wavelength
sensitive cone
pigment): It
absorbs
maximally in a
yellow position
with a peak of
565 nm. But its
spectrum
extends far
enough in to
the long
wavelength to
sense red.

8. GREEN SENSITIVEGREEN SENSITIVE
CONECONE PIGMENTPIGMENT ––
((ChlorolabeChlorolabe or mediumor medium
wavelength sensitive conewavelength sensitive cone
pigment): It absorbspigment): It absorbs
maximally in themaximally in the greengreen
portionportion with peak atwith peak at 535 nm.535 nm.
BLUE SENSITIVE CONEBLUE SENSITIVE CONE
PIGMENTPIGMENT (Cyanolabe):(Cyanolabe):
short wavelength sensitiveshort wavelength sensitive
(SWS) cone pigment absorbs(SWS) cone pigment absorbs
maximally in the blue – violetmaximally in the blue – violet
portion of the spectrum with aportion of the spectrum with a
peak atpeak at 420 nm420 nm

9.  Ewald Hering
 some colours are mutually exclusive
 Early recordings of the responses of
single neurons in primate retina and
geniculate nucleus revealed that-
 Cells excited by red and inhibited
by green light or vice versa. These
were thought to be the red/green
opponent color channel of Hering.
 blue/yellow channel of Hering.
 Hering's white/black channel
Ewald HeringEwald Hering

10.  The trichromatic theory by
itself was not adeqaute to
explain how mixture of lights
of different colours could
produce lights and yet another
colour or even to appear
colorless. So both the theories
are useful in that.
 The colour vision is
trichromatic at the level
of photoreceptor and
 Colour opponency is
explained by
subsequent neural
processing.

11. Cones differ from rods only
in opsin part c/a photopsin.
The green sensitive and red
sensitive cone pigments-
96% homology of amino
acid sequence.
Where each of these
pigments has only about
43% homology with the
opsin of blue sensitive cone
pigment.
All three bleached by light of
different wavelength.

12. Genesis of visual signal-
The photochemical changes
in cone pigments is
followed by a cascade of
biochemical cone receptor
potential.
Sharp onset and offset.

13. action potential generated in
photoreceptors
bipolar cells and horizontal cells
ganglion cells and amacrine cells.
synapses
synapses

14. It shows two complete different kind
of response.
 Luminosity Response : hyperpolarising
response.
 Chromatic Response : hyperpolarizing
in a part of spectrum and depolarising
for the remainder of the spectrum.
 This two response provide the first physiologicalThis two response provide the first physiological
evidence of opponent colour coding and it alsoevidence of opponent colour coding and it also
represents the first stage in visual system whererepresents the first stage in visual system where
evidence of chromatic interaction has been foundevidence of chromatic interaction has been found
and where wavelength discrimination can occur.and where wavelength discrimination can occur.

15.  BIPLOAR CELL : It shows the centre surround
spatical pattern. Red light striking in the centre
of this cell causes hyperpolarisation and green
light in the surrounding causes depolarization.
 AMACRINE CELLS: The exact role is not known
but they may act as an automatic colour
control.

16.  three types- W, X and Y
 X ganglion cell mediate the color sensation.
 A single ganglion cell may be stimulated by a
number of cones or by a few cones.
When all the three types of cones (Red, Green
and Blue) stimulate the same ganglion cell the
resultant signal is white.

17. Some of the ganglion
cells are excited by
one colour type cone
and are inhibited by
other. This system is
called ‘Opponent
colour cell” System
and concerned in the
successive colour
contrast.

18. These ganglion cells
have a system which is
opponent for both
colour and space. This
system is called
‘Double opponent cell
system and is
concerned with the
simultaneous colour
contrast.

20. (S+L)-M=RED
+ -
M-(S+L)=GREEN

21. +
(S+M)-L=BLUE (L+M)-S=YELLOW

22.  Trichromatic colour
vision mechanism extends
20 – 30° from the point of
fixation. Peripheral to this
red and green become
indistinguishable and in
the far periphery all colour
sense is lost.
 The very centre of
fovea is blue blind.

23. All LGB neurons carry
information from more
than one cone cells.
Colour information
carried by ganglion cell is
relayed to the
parvocellular portion of
LGB.

24. Spectrally non opponent
cell which give the same
type of response to any
monochromatic light
constitute about 30% of
all the LGB neurons.
Spectrally opponents
cells make 60% of LGB
neurons these cells are
excited by some
wavelength and inhibited
by others and thus
appear to carry colour
information

25. Colour information
parvocellular portion of the
LGB
layer IVc of striate cortex
(area 17).
blobs in the layers II and III
thin strip in the visual
association area
lingual and fusiform gyri of
occipital lobe.( specialized
area concerned with colour)
Analysis of colour
signals in the visual
cortex

26.  SIMULTANEOUS COLOUR
CONTRAST:
 perception of particular
coloured spot against the
coloured back ground.
 The colour of the spot tends
to be complementary
towards the colour of the
surround.
 function of double
opponent cells .

27. Successive colour contrast is the effect of
previously-viewed color fields ("inducing
fields") on the appearance of the currently-
viewed test field.
 it is a phenomenon of coloured after image.
It is function of opponent cell of visual system.

28. An afterimage or ghost image is an optical
illusion that refers to an image continuing
to appear in one's vision after the exposure
to the original image has ceased

29. In which the human eye
continue to perceive the
colour of a particular
object unchanged even
after the spectral
composition of the light
falling on it is markedly
altered.
 Computational
mechanism of brain is
responsible for this
phenomenon.

30. HUE- Identifiction of
color
BRIGHTNESS-
Intensity of color
SATURATION-
Purity of color

31.  HUE : Is the dominant
spectral colour is
determined by the
wavelength of the
particular colour. Hue is
that aspect of colour
describe with the names
such as red, blue, green
etc.

32. BRIGHTNESS: depends upon the
luminosity of the component
wavelength.
 In photoptic vision-peak
luminosity function at
approximately 555 nm and in
scotopic vision at about 507 nm.
 The wavelength shift of
maximum luminosity from
photoptic to scotopic viewing is
called ‘ Purkinje Shift
Phenomenon’

33. SATURATION : it refers to degree
from freedom to dilution with
white.
 It can be estimated by
measuring how much of a
particular wavelength must be
added to white before it is
distinguishable from white.
 The more the wavelength
require to be added to make the
discrimination, the lesser the
saturation.

34. COLOUR BLINDNESS
 Is the inability to perceive difference
between some of the colours that other
people can distinguish.
 The first major study of colour blindness
was published in 1794 by John Dalton,
who was colour-blind.
 colour blindness is sometimes called
“Daltonism”,
 Defective perception of colour
(anomalous) and absent of colour
perception is anopia.
 It may be-
 Congenital
 Acquired
John Dalton

35. X – linked recessive
 Affecting males more (3 –
4%) than female (0.4%)
 Types
 Dyschromatopsia
 Achromatopsia
 Dyschromatopsia: colour
confusion due to deficiency
of mechanism to perceive
colours. 2 types:
 Anomalous trichromatism
 Dichromatism

36. Here the mechanism to
appreciate all the three primary
colour is present but is defective
for one or two of them.
TYPES-
 PROTANOMALOUS:PROTANOMALOUS:
 DEUTERANOMALOUS:DEUTERANOMALOUS:
 TRITANOMALOUS:TRITANOMALOUS:
Red- green deficiency is most commonRed- green deficiency is most common
Blue deficiency is comparatively rareBlue deficiency is comparatively rare

37. B. DICHROMATE COLOUR
VISION: Means faculty of
perceive one of the three primary
colours is completely absent.
Protanopia: complete red
colour defect
Deuteranopia: complete defect
of green colour
Tritanopia: Absence of blue of
colour appreciation
PROTANOPIA. TRITANOPIADEUTERANOPIA

39.  Extremely rare
condition
2 types
 cone
monochromatisn
 rod monochromatisn
Cone
Monochromatism:
Presence of only one
primary colour.
 visual acquity of 6/12
or better.

40.  very rare
complete or incomplete
 autosomal recessive trait.
Characterized by:
• Total color blindness
• Day blindness (V.A.
about 6/60)
• Nystagmus
• Fundus is usally normal

41. Red, green
and blue
cone
sensitivity vs.
wavelength
curves

42. Red or green cone peak
sensitivity is shifted.
or
Red or green cones absent

43. B RG
437 nm 564 nm
533 nm
NORMAL CONE
SENSITIVITY CURVES
(TRICHROMAT)

44. 5% of Males
B RG
437 nm 564 nm
Deuteranomaly
(green shifted toward red)

45. 1% of Males (there is no green curve)
B R
437 nm 564 nm
Deutan Dichromat
(no green cones; only red
and blue)

46. B RG
437 nm
533 nm
1% of Males
Protanomalous
(red shifted toward green)

47. 1% of Males (there is no red
curve)
B G
437 nm
533 nm
Protan Dichromat
(no red cones; only green
and blue)

48. Why do colors
that look different
to us appear the
same to color
deficient
individuals?

49. Consider a green vs.
yellow light…
B RG
Large
difference in
stimulation of
green and red
cones
Small
difference in
stimulation
The two spots appear
different in color because R-
G is large for one, and small
for the other.

50. Each spot produces the
same R-G stimulation and
thus looks the same!
B RG
Small
difference
in
stimulation
 Look the same!
Small difference in
stimulation
Deuteranomaly
(the green sensitivity curve is
shifted toward the red)

51. Color Deficiency Males Females
Protanopia 1% 0.01%
Deuteranopia 1% 0.01%
Protanomaly 1% 0.01%
Deuteranomaly 5% 0.4%
Overall (red-green) 8% 0.5%
Tritanopia 0.008% 0.008%
Tritanomaly Rare Rare
Rod
monochromatism
Rare Rare
Cone
monochromatism
Rare Rare

52.  ACQURIED COLOUR BLINDNESS
 Koelhar formulated that lesions in the outer layers
of retina give rise to a blue yellow defect, while
lesion in the inner layer & optic nerve may produce
red-green defect.
 Blue yellow impairment: is usually seen in
 Central serous retinopathy
 Diabetic retinopathy
 Macular oedema
 Myopia
 Retinitis pigmentosa
 Red green deficiency
 Optic neuritis
 Leber’s optic atrophy

53. Acquired blue colour defect: crystalline lens
absorbs shorter wavelength in young, less than
400 nm and in old people up to 550 nm are
absorbed. It results in defective colour vision on
shorter wavelength side.
DRUG CAUSING CVD
Blue-yellow: chloroquine, indomethacin, oral
contracaptives. Estrogens, Digitalis & Butazolidin
Red green: Ethyl alcohol & Ethambutol
Mixed type: Di & Tri cyclic anti depressants.

54.  Gene rhodopsin -
chromosome 3.
 Gene for blue sensitive
cone - chromosome 7, AD
 The genes for red and
green sensitive cones are
arranged in tandem array
on the ‘q’ arm of x
chromosome,XR.
 Tritanopia and tritanomaly
– rare,no sexual
selectivity.

55. DEUTERANOMALY AND
PROTANOMALY
 Is probably due to the
arrangement of the genes for
the green and red sensitive cone
pigments.
 They are located near each
other in a head to tail tandem
array on the ‘q’ arm of the X
chromosome and are prone to
recombination during
development of germ cell.

56.  PSEUDOISOCHROMATIC
COLOUR TEST:
most commonly employed
tests- eg.-
ISHIHARA PLATES

and
HRR(HARDY,RAND,RITTLER)
plates
 Ideal for paediatric testing of
congenital color blindness.

57. designed in four ways
1st
plate-
 for demonstration and
malingerers.

58. (2-9) plate-
Transformation plates:
normal person sees one
figure and a CVD sees
another.
 (10-17)plate-Vanishing
plates: normal person see
the figure while a CVD
person will not

59. Pseudoisochromatic colour
plates
(18-21)plate-Hidden-digit
plates: normal person
does not see a figure while
a CVD will see the figure.
(22-25)plate-Diagnostic
plates: seen by normal
subjects, CVD one number
more easily than another.
Protans only see the no. on
the right side and deutans
only see the no. on the
left.
75 cm ,day light,right
angle,3 sec.

60. For illitrate patients

62. subject has to name the
various colours shown to
him by a lantern.
TYPES:
 Farnsworth lantern
 Optec 900
 Holmes Wright Type A and
B lantern
 Beyne lantern
Edridge green lantern is
most popular test.

63. MOST SENSITIVE.
Subject has to
arrange 85 colour
chips in ascending
order.
 The colour vision
is judged by the
error score.
 The results are
recoded in a circular
graph.

64. Normal pattern Abnormal patterns

65. Abridged
version
Patients are
asked to
arrange 15
coloured caps
in sequential
order based on
similarity from
the pilot colour
cap .

66. 10 Plates ,35
cm,daylight,right
angle.
It is also a
spectroscopic test
where a centre
coloured plate is to
be matched to its
closest hue from
four surrounding
colour plates.

67. The subject is asked
to make a series of
colour matches from a
selection of skeins of
coloured wools.

68. GOLD STANDARD
Extraordinarily sensitive.
 In this test the observer
is asked to mixed red and
green colours in such a
proportion that the
mixture should match the
yellow colour disc.
 Indication of defect is
relative amount of red and
green required.

70. MOST RELIABLE means
to distinguish acquired
from inherited color
vision defect.
Not commercially
available.

71. Color blindness
no yes
Red-green Blue-yellow
Protan Deutan
Genetic Acquired
Anamolous Anamoly
mild moderate severe

72.  Currently No treatment.
 Some filters may help to distinguish the colours
but not in the identification of colours.
 The purpose of this is to eliminate certain lights
and modify the light reaching the eyes so that the
receptors receive correct information.
Future direction-
Viral mediated gene
therapy

73. Tinted contact lenses
Filtered goggles

74. REFFERENCES
 Diagnosis of Defective
Colour Vision – Jennifer
Birch 2nd
ed.
 Clinical neuro-
ophthalmology-Ulrich
schifer
 Ophthalmology – Myron
Yanoff & jay s. Duker 2nd
ed
 Clinical ophthalmology –
Jack J. Kanski 6th
ed.
 Adler’s Physiology of Eye
19th
ed.
 Parson’s Basic Diseases of
The Eye- 20th
ed.